Interactive Cardiovascular and Thoracic Surgery 3:121-123(2004)
© 2004 European Association of Cardio-Thoracic Surgery
Negative results - Cardiac general |
Heparin induced thrombocytopenia type II complicating coronary artery bypass surgery: a tale of caution
Uday Dandekar*,
Jonathan Young,
Maninder Kalkat and
Christopher M.R. Satur
Department of Cardiothoracic Surgery, North Staffordshire Royal Infirmary, Princes Road, Hartshill, Stoke-on-Trent, ST4 7LN, UK
* Corresponding author. Tel.: +44-778-6824219; fax: +44-1782 555058
udandekar{at}yahoo.co.uk
Received June 19, 2003;
received in revised form September 20, 2003;
accepted September 23, 2003
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Abstract
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Objective: To highlight an uncommon problem of heparin induced thrombocytopenia after coronary artery bypass operation. Methods: We report the case of a 59-year-old man who suffered severe type II heparin induced thrombocytopenia (HIT) after coronary artery bypass operation. He experienced extensive skin necrosis at sites of saphenous vein harvesting, which progressed to cause soft tissue necrosis of both feet. He also exhibited secondary clinical features arising from pulmonary, hepatic and renal dysfunction suggestive of extensive venous thrombosis. Primary treatment of the haematological disorder was achieved by discontinuation of all forms of heparin and the administration of a heparinoid intravenously. Secondary treatment included forefoot amputations and skin grafting. Results: Though the patient suffered a protracted period of recovery he was discharged home well. Conclusion: We have reported this complex case in order to familiarise cardiothoracic surgeons with the extreme characteristics of type II HIT and to emphasise that early diagnosis and treatment will facilitate a successful outcome.
Key Words: Heparin induced thrombocytopenia; Cardiac surgery
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1. Introduction
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HIT may be diagnosed in 1.9% of patients following cardiac surgery, but only 4–5% patients suffer the complications of type II HIT [1,2]. It is characterised by extensive venous and arterial thrombosis, with a mortality of approximately 33%. We report the case of a survivor who overcame the extensive systemic failure that accompanied the condition. This case highlights the clinical picture and shows that early diagnosis and treatment may be accompanied by a successful outcome.
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2. Case report
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A 59-year-old male, insulin dependant diabetic and smoker, suffered an acute myocardial infarction complicated by pulmonary oedema. He was treated by thrombolysis and prophylactic anticoagulation with heparin. Cardiac catheter demonstrated severe triple vessel coronary artery disease and poor ventricular function. He was admitted electively and received a quintuple coronary artery bypass operation. Grafts included the left internal thoracic artery and long saphenous vein, and cardiopulmonary bypass was utilised with heparin anti-coagulation. Treatment in the postoperative period included prophylactic subcutaneous heparin. Recovery was rapid and uneventful. He was discharged on the 6th postoperative day when a platelet count was recorded at 194,000/µl.
He was awoken on the 11th postoperative night by intense pain in his legs and found that the wounds of the graft donor sites were surrounded by a 3-cm margin of black skin. Following admission to a district hospital and later to our unit, extensive skin blistering necrosis was confirmed (Fig. 1). Areas of necrosis also surrounded intravenous cannulation sites and sites of subcutaneous heparin administration. The sternotomy wound was entirely spared. Haematological investigations demonstrated a platelet count reduced to 34,000/µl, serum D-Dimer concentration >8000 ng/ml (normal <250 ng/ml), and platelet destruction on a blood film. A presumptive diagnosis of disseminated intravascular coagulation (DIC) accompanying synergistic infective necrotising epidermolysis was made.
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Fig. 1 Photograph showing extensive superficial skin necrosis and blistering surrounding saphenous vein donor site.
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Over subsequent days the area of skin necrosis extended to involve the soft tissue of both feet despite normal pedal pulses indicating the cause to be venous gangrene. Serious systemic dysfunction followed. Frank haemoptysis, dyspnoea and marked hypoxia occurred and a chest X-ray demonstrated opacification of the right lower lobe of lung suggestive of a pulmonary infarct (Fig. 2). His poor condition prevented investigation with an isotope lung scan. Hepatic dysfunction was demonstrated by a rise in of serum enzymes, the serum alanine transaminase to 853 µ/l (normal 0–40 µ/l) and renal dysfunction by a serum creatinine of 201 µmol/l. The platelet count had deteriorated to a minimum of 15,000/µl.
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Fig. 2 Chest X-ray showing right lower lobe lung opacification suggestive of a pulmonary infarct and right pleural effusion.
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In view of the extensive venous thrombosis and accompanying thrombocytopenia the diagnosis was reviewed and HIT diagnosed by demonstration of the presence of anti-heparin antibodies in the serum. All forms of heparin administration were discontinued and an infusion of Danaparoid (Durbin PLC, Middlesex, UK) commenced. Over a period of 5 days the blood platelet count returned to normal. Further anti-coagulation was achieved by treatment with oral warfarin. Resolution of the pulmonary, renal and hepatic dysfunction were protracted but complete. Extensive plastic repair of the limb necrosis by excision of eschar and bilateral forefoot amputations, and by secondary skin grafting. He was, however, discharged home well.
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3. Comment
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We have reported this case in order to bring to the attention of cardiothoracic surgeons the rare but malevolent nature of type II HIT in contrast to the benign nature of the more commonly witnessed type I HIT. HIT is characterised by a decrease in platelet count following the administration of heparin. Its incidence is reported to be 5–30%, but has affected only 1.9% of cardiac patients [1,3,4]. The subgroup type I or non-immune HIT, accounts for 95–96% of cases, and is attributed to the pro-aggregatory effect of heparin on platelets. The platelet count decreases whilst heparin is administered to a nadir of 100,000/µl, and returns to normal regardless of whether or not heparin is continued [2,5,6].
HIT type II presents after an interval of 3–15 days of the commencement of heparin therapy and is an immunlogically mediated via IgG antibodies that target the heparin-platelet complex. Activation of the platelets by the antibodies triggers platelet lysis and secondary aggregation and thrombosis [6]. The platelet count decreases to below 100,000/µl. Its complications include haemorrhage, thromboembolism and death in 53%, 44%, and 33% of patients, respectively [1].
Acute treatment is achieved by cessation of all forms of unfractionated and fractionated heparin administration and by intravenous administration of heparinoids that arrest the thrombocytopenia. Subsequent anti-coagulation should be provided with warfarin. The anti-platelet antibody reaction is transient and may disappear by 4–8 weeks, and if required exposure to heparin may be undertaken after this interval, though it is recommended that the alternative agents, i.e. heparinoids, should be used [7].
This case presented characteristic features of type II HIT. Symptoms succeeded two episodes of exposure to heparin, firstly following the myocardial infarction and secondly during and after coronary surgery, but after all therapy had been discontinued. The interval between presentation and heparin exposure may be attributed to delayed production of antibodies. Venous thrombosis caused gangrene of the lower limbs and the central organ dysfunction occurred presumably secondary to central venous thrombosis. Lastly the occurrence of HIT was confirmed by the demonstration of anti-platelet anti-bodies. Treatment was successfully initiated by the administration of intravenous danaparoid and by discontinuing all forms of heparin. Despite the rapid return to normal of the platelet count the results of extensive ischaemic injury required extensive plastic surgical therapy over a matter of months.
Severe pain was a clinical problem, the management of which was made problematic by the haematological features of HIT. Intravenous opiates provided marginally effective analgesia but caused respiratory depression and exacerbated the pulmonary dysfunction. Use of non-steroidal analgesics were contraindicated by the thrombocytopenia of 15,000/µl, as was epidural analgesia. Femoral nerve blockade with bupivacaine did, however, prove to be beneficial.
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4. Conclusion
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Whilst HIT type II is a rare complication of heparin therapy, its devastating effects may be successfully treated the early institution of heparinoid therapy. Early diagnosis and intensive therapy are essential to achieve a successful resolution of the problem.
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Appendix A
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ICVTS on-line discussion
Author: Dr. Hitoshi Hirose, Cleveland Clinic Foundation, Cardiovascular Surgery, 2300 Overlook Rd #312, Cleveland, OH 44106, USA
Date: 10-Dec-2003
Message: Heparin induced thrombocytopenia (HIT) usually presents with symptoms and signs of distal artery occlusive symptom (such as cyanotic and cool foot or hand), or vent thrombosis (upper or lower extremity deep vein thrombosis) associated with thrombocytopenia; however, the wound necrosis is a rare presentation. I agree with the authors that early diagnosis of HIT, discontinuation of heparin, and early treatment with direct-thrombin inhibitor (argatoban or lepirudin) are essential. The later the treatment is begun, the worse the outcome is going to be.
doi:10.1016/S1569-9293(03)00231-7
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References
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- Ralph-Edwards AC, Feindel CM, Glynn MF. Successful treatment of massive pulmonary embolism after coronary artery bypass grafting due to heparin-induced thrombocytopenia. Ann Thorac Surg 1994;57:1326–8.
- King DJ, Kelton JG. Heparin-associated thrombocytopenia. Ann Intern Med. 1984;100:535–540[Abstract/Free Full Text]
- Mehta DP, Yoder EL, Appel J, Bergsman L. Heparin-induced thrombocytopenia and thrombosis: reversal with streptokinase: a case report and review of literature. Am J Hematol. 1991;36:275–279[Medline]
- Singer RL, Mannion JD, Bauer TL, Armenti FR, Edie RN. Complications from heparin-induced thrombocytopenia in patients undergoing cardiopulmonary bypass. Chest. 1993;104:1436–1440[Abstract/Free Full Text]
- Fabrizio F, Schmidt CA. Cardiopulmonary bypass in patients with heparin-induced thrombocytopenia and thrombosis. Ann Thorac Surg. 2000;70:2173–2181[Abstract/Free Full Text]
- Olinger GN, Hussey CV, Olive JA, Malik MI. Cardiopulmonary bypass for patients with previously documented heparin-induced platelet aggregation. J Thorac Cardiovasc Surg. 1984;87:673–677[Abstract]
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Abstract
1. Introduction